Breaking anergy

B cells made anergic by chronic exposure to a self antigen are able to be activated in some instances. As indicated above, stimulation of anergic B cells through the CD40 molecule in the presence of IL-4 is able to induce proliferation and differentiation of the B cell. Similarly, extensive cross-linking of surface immunoglobulin on the B cell is able to activate the cell. This can be achieved, for example, when a B cell chronically exposed to soluble monomeric self antigen encounters the same antigen in a highly multimerized form such as a cell protein. In this case, the B cell will proliferate and differentiate into an antibody-forming cell in the presence of the appropriate cofactors. This reversal of anergy is dependent on the strength of the receptor signal. In the presence of soluble self antigen, anergic B cells are killed by antigen specific nontolerant helper T cells. This death is dependent on anergic B cells expressing the apoptosis-inducing molecule Fas and the helper T cells expressing its ligand. This lethal embrace can be transformed into a stimulatory one if the antigen receptor stimulation given to the B cell is sufficiently strong.

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